Extracellular vesicle signalling in atherosclerosis

Charla, Eleni; Mercer, John R.; Maffia, Pasquale; Nicklin, Stuart A.

doi:10.1016/j.cellsig.2020.109751

Cited by 37 publications

(33 citation statements)

References 216 publications

(304 reference statements)

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“…C1QA, FGG, FN1, and VWF could therefore be involved in atherogenesis progression in patients with CSC ischaemic stroke. These results agree with those of previous studies that determined that the EV cargo is implicated in atherosclerosis development, including immune responses, cell proliferation and migration, cell death, and vascular remodelling during disease progression [35]. This characteristic of the EV cargo in CSC ischaemic stroke might be due to the fact that most infarctions that affect the cortical and subcortical areas are large vessel strokes whose main aetiology is atherosclerosis.…”

Section: Cargo Of Circulating Extracellular Vesicles In Cortical-subcortical Ischaemic Strokesupporting

confidence: 92%

Circulating Extracellular Vesicle Proteins and MicroRNA Profiles in Subcortical and Cortical-Subcortical Ischaemic Stroke

et al. 2021

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In order to investigate the role of circulating extracellular vesicles (EVs), proteins, and microRNAs as damage and repair markers in ischaemic stroke depending on its topography, subcortical (SC), and cortical-subcortical (CSC) involvement, we quantified the total amount of EVs using an enzyme-linked immunosorbent assay technique and analysed their global protein content using proteomics. We also employed a polymerase chain reaction to evaluate the circulating microRNA profile. The study included 81 patients with ischaemic stroke (26 SC and 55 CSC) and 22 healthy controls (HCs). No differences were found in circulating EV levels between the SC, CSC, and HC groups. We detected the specific expression of C1QA and Casp14 in the EVs of patients with CSC ischaemic stroke and the specific expression of ANXA2 in the EVs of patients with SC involvement. Patients with CSC ischaemic stroke showed a lower expression of miR-15a, miR-424, miR-100, and miR-339 compared with those with SC ischaemic stroke, and the levels of miR-339, miR-100, miR-199a, miR-369a, miR-424, and miR-15a were lower than those of the HCs. Circulating EV proteins and microRNAs from patients with CSC ischaemic stroke could be considered markers of neurite outgrowth, neurogenesis, inflammation process, and atherosclerosis. On the other hand, EV proteins and microRNAs from patients with SC ischaemic stroke might be markers of an anti-inflammatory process and blood–brain barrier disruption reduction.

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Section: Cargo Of Circulating Extracellular Vesicles In Cortical-subcortical Ischaemic Strokesupporting

confidence: 92%

Circulating Extracellular Vesicle Proteins and MicroRNA Profiles in Subcortical and Cortical-Subcortical Ischaemic Stroke

et al. 2021

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“…EVs and plaque stability/instability. Reportedly, the EVs present in atherosclerotic plaques are involved in cellular signaling, atherosclerosis development, immune responses, inflammation, cell proliferation and migration, cell death and vascular remodeling during the progression of the disease [ 89 ]. One mechanism by which EVs contribute to the stability of the atherosclerotic plaque is their implication in vascular calcification.…”

Section: Extracellular Vesicles Have the Potential To Predict Monitor And Act As Therapeutic Agents In Atherosclerosismentioning

confidence: 99%

Extracellular Vesicles: Versatile Nanomediators, Potential Biomarkers and Therapeutic Agents in Atherosclerosis and COVID-19-Related Thrombosis

Georgescu

Simionescu

2021

IJMS

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Cells convey information among one another. One instrument employed to transmit data and constituents to specific (target) cells is extracellular vesicles (EVs). They originate from a variety of cells (endothelial, immune cells, platelets, mesenchymal stromal cells, etc.), and consequently, their surface characteristics and cargo vary according to the paternal cell. The cargo could be DNA, mRNA, microRNA, receptors, metabolites, cytoplasmic proteins, or pathological molecules, as a function of which EVs exert different effects upon endocytosis in recipient cells. Recently, EVs have become important participants in a variety of pathologies, including atherogenesis and coronavirus disease 2019 (COVID-19)-associated thrombosis. Herein, we summarize recent advances and some of our own results on the role of EVs in atherosclerotic cardiovascular diseases, and discuss their potential to function as signaling mediators, biomarkers and therapeutic agents. Since COVID-19 patients have a high rate of thrombotic events, a special section of the review is dedicated to the mechanism of thrombosis and the possible therapeutic potential of EVs in COVID-19-related thrombosis. Yet, EV mechanisms and their role in the transfer of information between cells in normal and pathological conditions remain to be explored.

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“…The role of EVs in atherosclerosis, especially platelet EVs, has been already investigated and described in several reviews (Charla et al., 2020; Oggero et al., 2019; Van Der Vorst et al., 2018). However, as a relevant example, a recent publication by Zaldivia et al.…”

Section: Discussionmentioning

confidence: 99%

Extracellular vesicles from monocyte/platelet aggregates modulate human atherosclerotic plaque reactivity

Oggero

Gaetano

Marcone

et al. 2021

J of Extracellular Vesicle

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Extracellular vesicles (EVs) are emerging as key players in different stages of atherosclerosis. Here we provide evidence that EVs released by mixed aggregates of monocytes and platelets in response to TNF‐α display pro‐inflammatory actions on endothelial cells and atherosclerotic plaques. Tempering platelet activation with Iloprost, Aspirin or a P2Y12 inhibitor impacted quantity and phenotype of EV produced. Proteomics of EVs from cells activated with TNF‐α alone or in the presence of Iloprost revealed a distinct composition, with interesting hits like annexin‐A1 and gelsolin. When added to human atherosclerotic plaque explants, EVs from TNF‐α stimulated monocytes augmented release of cytokines. In contrast, EVs generated by TNF‐α together with Iloprost produced minimal plaque activation. Notably, patients with coronary artery disease that required percutaneous coronary intervention had elevated plasma numbers of monocyte, platelet as well as double positive EV subsets. In conclusion, EVs released following monocyte/platelet activation may play a potential role in the development and progression of atherosclerosis. Whereas attenuating platelet activation modifies EV composition released from monocyte/platelet aggregates, curbing their pro‐inflammatory actions may offer therapeutic avenues for the treatment of atherosclerosis.

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Extracellular vesicle signalling in atherosclerosis

Cited by 37 publications

References 216 publications

Circulating Extracellular Vesicle Proteins and MicroRNA Profiles in Subcortical and Cortical-Subcortical Ischaemic Stroke

Circulating Extracellular Vesicle Proteins and MicroRNA Profiles in Subcortical and Cortical-Subcortical Ischaemic Stroke

Extracellular Vesicles: Versatile Nanomediators, Potential Biomarkers and Therapeutic Agents in Atherosclerosis and COVID-19-Related Thrombosis

Extracellular vesicles from monocyte/platelet aggregates modulate human atherosclerotic plaque reactivity

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